Suprachoroidal Hemorrhage

From EyeWiki

Disease Entity

Suprachoroidal Hemorrhage


Suprachoroidal hemorrhage (SCH) is a rare, but potentially vision threatening pathology that may manifest as a consequence of intraocular surgery. It occurs when blood from the long or short ciliary arteries fills within the space between the choroid and the sclera.[1] Suprachoroidal hemorrhages are classified in several ways. They may be categorized with respect to size and the extent of hemorrhage, relationship to intraocular surgery (intraoperative/expulsive or postoperative/delayed), or precipitating events (spontaneous, blunt/penetrating trauma or perioperative).[2] Chu et al notes that traumatic SCH behave differently from perioperative SCH and “should be considered a distinct entity.”[2] This report will focus mostly on SCH as it pertains to intraocular surgery.

Risk Factors

There are several characteristics from the patient's medical and ocular history, and intraoperative and postoperative management that increase the relative risk for perioperative SCH.

Systemic risks [1]

  • Advanced age
  • Use of anticoagulant or antiplatelet medications
  • Uncontrolled hypertension
  • Atherosclerosis
  • Diabetes

Ocular risks [1][3]

  • History of glaucoma
  • High myopia
  • Aphakia
  • Previous ocular trauma
  • Previous intraocular surgery
  • History of SCH
  • Choroidal hemangioma
  • Elevated preoperative intraocular pressure (IOP).

Intraoperative risks [1][3]

  • General and retrobulbar anesthesia
  • Valsalva-type maneuvers (including “bucking” under general anesthesia)
  • Hypotony or acute drop in IOP
  • Prolonged or complicated eye surgery (including vitreous loss during cataract surgery)

Postoperative risks [1]

  • Hypotony
  • Valsalva maneuvers
  • Emesis


Although there are several theories regarding the mechanism by which SCHs develop, the overarching theme is hypotony or low IOP.[2] Hypotony causes long or short posterior ciliary arteries to rupture leading to hemorrhage within the space between the choroid and the sclera.[2] The current debate is whether preexisting damage to the posterior ciliary arteries increases their susceptibility to rupture during times of stress or hypotony causes a significant choroidal effusion that stretches and ruptures the arteries.[2][3] Histopathologic studies lends more evidence to the latter,[3] but SCH, most likely, is a combination of both mechanisms.[2][4]


The incidence of spontaneous SCH is not known because it occurs very rarely. A 1999 study by Chu et al performed the most extensive retrospective literature review in the past 25 years of the major ophthalmologic surgeries where SCHs occurred.[2] They found that risk was higher for patients undergoing glaucoma surgery (range: 0.15% to 6.1%) and vitreoretinal surgery (range: 0.17% to 1.9%) and lower in those having penetrating keratoplasty (range: 0.087% to 1.08%) or cataract surgery (range: 0.03% to 0.81%).[2][4]

Primary prevention

The aim of primary prevention is to mitigate or eliminate the modifiable risk factors discussed above. Therefore, in the preoperative period, it is recommended that patients undergo complete ophthalmic and medical evaluation, manage comorbidities such as hypertension and diabetes, avoid antiplatelet and anticoagulation medications, and minimal phenylephrine use.[2] During ophthalmic surgery, physicians may further decrease the risk of suprachoroidal hemorrhages by using local instead of global anesthesia whenever possible, lowering IOP before incision, avoiding rapid decompression of the globe, and avoiding patient Valsalva maneuvers.[2] Lastly, in the postoperative period, patients should avoid eye trauma, extensive eye pressure, hypotony, and Valsalva maneuvers.[2]


Signs and Symptoms

As discussed earlier, SCH’s most commonly occur either intraoperatively or postoperatively. Interestingly, the type of intraocular surgery is a significant determinant of when it occurs -- cataract surgery tends to cause intraoperative SCH’s while glaucoma surgery tends to cause postoperative SCH’s.[1][5] [6] Nonetheless, the signs and symptoms are relatively independent of time of initial presentation.

Intraoperative signs of SCH may include [1][2]

  • Anterior chamber shallowing
  • Loss of the red reflex
  • Increased IOP with or without firming of the eye
  • Wrinkling and bulging of the posterior capsule
  • Extrusion of intraocular contents: spontaneous nuclear expression, iris prolapse, and vitreous prolapse

Postoperative signs and symptoms of SCH may include [1][2]

  • Severe eye pain, headache, nausea with or without vomiting that are typically worse with Valsalva maneuvers
  • Decreased visual acuity
  • Anterior chamber shallowing
  • Loss of the red reflex
  • Elevated IOP
  • Vitreous prolapse into the anterior chamber
  • Choroidal elevation


Although SCH may be diagnosed clinically, it is typically beneficial for an ophthalmologist to obtain imaging to help rule out other pathologies, direct treatment, and monitor progress. Sometimes SCH’s are difficult to diagnose in the postoperative period, especially in the presence of opacifications that obscure adequate visualization. The typical multimodal imaging techniques that may be helpful are fluorescein angiography (FA), indocyanine green angiography (ICG), ultrasound B scan, optical coherence tomography (OCT), computed tomography (CT) and magnetic resonance imaging (MRI).[2][7] FA and ICG are typically normal in SCH and therefore may assist in ruling out other pathologies. Ultrasonography (B scan and A scan) can help diagnose and direct management of SCH’s because it can determine the location and extent of the hemorrhage and the status of the retina and vitreous.[2]

Ultrasonography is crucial during the close follow up after the patient develops the suprachoroidal hemorrhage and also aids in the timing of any surgical intervention. The SCH typically has a dome shaped appearance. On A-scan, the (inner) wall of the SCH has a typical high reflectivity spike followed by a relatively lower spike in the suprachoroidal space indicating clotted hemorrhage. The density of the SCH will change over time and is excellent in following these patients. On B-scan ultrasound, the initial hyperechoic clots with irregular shape are followed by a hypoechoic and more homogenous appearance indicating clot breakdown and liquefaction. With mean clot lysis taking place somewhere between 7 and 14 days depending on the study, the use of ultrasonography is vital to the management of these complex patients. The liquefaction can also be demonstrated during follow up with dynamic ultrasonography. Also of importance is the monitoring of the height of the SCH itself. Documenting reduction in height is helpful in surgical decision making.

OCT is similar to ultrasound because it can also provide information on the location and extent of the hemorrhage. CT and MRI may provide information on the location and differentiation of various soft tissue, serous, and hemorrhagic pathologies that may not be shown in the imaging modalities previously discussed.[2]

Differential Diagnosis


  • Retrobulbar hemorrhage
  • Serous choroidal effusion


  • Retrobulbar hemorrhage
  • Acute angle closure glaucoma
  • Serous choroidal effusion
  • Posterior scleritis
  • Choroidal granuloma
  • Choroidal hemangioma


The first step in management of SCH is early recognition whether it be intraoperative or postoperative.


If an intraoperative SCH is suspected, immediate tamponade of bleeding vessels via direct pressure or closure of all incisions should be performed to prevent further hemorrhage and subsequent expulsion of intraocular contents.[2][4] If ocular contents are expelling, they should be put back in a timely fashion.[2] If the contents cannot be replaced, then drainage of the uncoagulated blood is necessary to help soften the eye.[2][8] Other indications for immediate drainage include retained lens material or retinal detachment.[8] Traditionally, drainage was achieved by posterior sclerotomies, but the long term benefits of this procedure are highly debated.[2] Rezende et al. suggests intraoperative SCH drainage via transconjunctival 25-gauge trocar insertion because it eliminates the need for simultaneous pars plana vitrectomy unless warranted for other concomitant pathologies.[9] The primary concern about immediate intraoperative SCH draining is allowing further bleeding to take place due to dislodging of the forming clot.

Once the hemorrhage and reposition of expulsed ocular contents are managed, the anterior chamber must be reformed via injection of either a viscoelastic agent or air to prevent entrapment of vitreous into the surgical wound.[2][4]

In complex cases where unsuccessful drainage the suprachoroidal blood occurred, there are techniques to help facilitate the process. One approach is to increase or maintain high IOP via limbal infusion, anterior chamber maintainer, or a long pars plana infusion to promote flow through the drainage system.[4] Another method is injection of a heavy liquid, perfluorocarbon liquid (PFCL), to help force blood out of the suprachoroidal space.[4]

Once in the postoperative phase, it is important to control the IOP with a topical beta blocker and an oral carbonic anhydrase inhibitor as necessary.[2] Topical steroids are prescribed to decrease ocular inflammation.[2] Topical cycloplegics and are prescribed to decrease ocular pain by preventing iris-corneal or lens-corneal touching. Oral analgesics may be prescribed to treat ocular pain.[10] However, aspirin and NSAIDS are contraindicated because their antiplatelet function may promote continued hemorrhage. Ultrasound B scans are typically used to follow patients to monitor the status of the SCH.


If SCH occurs postoperatively, the management approach is controversial. There is evidence for both non-surgical and surgical intervention.

Non-surgical management similar to the postoperative phase described above. Increased IOP should be treated with topical beta blocker.[2] [3][10] Ocular inflammation should be addressed with topical steroids.[2] [3][10] Ocular pain should be managed with topical cycloplegics, particularly atropine, and oral analgesics.[2] [3][10][11] As mentioned above, patients should receive serial ultrasound B scans of the affected eye in order to monitor progression of the SCH and help determine apposition, height, liquefaction of the SCH, and possible presence of a retinal detachment.

If the SCH does not resolve with medical management or severe ocular pain persists, then reoperation may be considered. Other indications for surgery include uncontrolled intraocular pressure, appositional, or "kissing" choroidals, and retinal detachment. As mentioned above, waiting clot lysis for proper liquefaction is very helpful to successful SCH drainage.

The main goals of reoperation is drainage of the SCH while allowing for proper maintenance of IOP.[8] Drainage is achieved with either one or two radial sclerotomies depending on SCH severity and patient response.[10] After proper establishment of IOP maintenance (usually provided by anterior chamber infusion due to inability to view the posterior placed infusion), one of two drainage methods are usually used: scleral cut down or trocar drainage. After conjunctival cutdown is created in the quadrant(s) with the highest elevated SCH, 3-4mm radial scleral cut downs are created, typically about 8mm posterior to the limbus. Gentle pressure at the edge of the sclerotomy can be held to allow ease of efflux of the SCH. Also, the use of forceps at the lip of one side of the cut down can allow for passage of clots (along with elevation of intraocular pressure). Transconjunctival trocar drainage may also be an option.[9] With newer valved trocars, ventilation is achieved with either forceps opening the valve or using a vent provided by the vitrectomy pack. Care must be taken with trocar drainage particularly at the time of trocar entry to ensure the quadrant the surgeon is entering is high enough that the the end of the trocar blade does not engage or pierce the RPE/retina. This is why this is typically done at an angle to avoid such a complication.

Traditionally, IOP is maintained with balanced salt solution, injection of gas, or a heavy liquid as described above.[4][8] However, Kurup et al. suggests that injection with viscoelastic may be more efficacious because it is retained in the vitreous more effectively keeping the IOP elevated and patients achieve better visual outcomes.[12]

However, if SCH is accompanied with retinal detachment, vitreoretinal traction, or vitreous hemorrhage then the drainage procedure may be combined with a vitrectomy or scleral buckle procedure.[2][8] Once proper drainage is achieved, posterior segment visualization can be attempted with direct viewing through additional trocars or indirect ophthalmoscopy to determine the need of additional vitreoretinal surgery to address other posterior segment pathology. The timing of re-operation remains up for debate. Some studies show that repairs within the first 36 hours successfully drain the SCH without reaccumulation of blood.[11] However, other studies report more complete drainage of SCH when reoperation occurs after 7-14 days because the extra time allows for clot lysis to occur.[11] Learned et al. compared results of several studies that evaluated either immediate or delayed drainage procedures and found that both are acceptable treatment options.[8]


The prognosis of both intraoperative and postoperative SCH is poor. An overwhelming majority of patients do not achieve pre-hemorrhage visual acuity and most do not recover to a visual acuity of 20/200 or better.[2] The major determinants of good or bad visual outcomes of SCH’s are preoperative visual acuity and retinal detachment at the time of hemorrhage, respectively.[13]


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  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 2.16 2.17 2.18 2.19 2.20 2.21 2.22 2.23 2.24 2.25 2.26 2.27 Chu TG, Green RL. Suprachoroidal hemorrhage. Surv Ophthalmol. 1999;43(6):471-486. doi: S0039625799000375 [pii].
  3. 3.0 3.1 3.2 3.3 3.4 3.5 3.6 Wolter JR, Garfinkel RA. Ciliochoroidal effusion as precursor of suprachoroidal hemorrhage: A pathologic study. Ophthalmic Surg Lasers Imaging Retina. 1988;19(5):344-349.{601a975b-b017-4ddd-863c-feaaf2e5c33a}/ciliochoroidal-effusion-as-precursor-of-suprachoroidal-hemorrhage-a-pathologic-study. Accessed May 13, 2020. doi: 10.3928/1542-8877-19880501-11.
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  6. Paysse E, Lee PP, Lloyd MA, et al. Suprachoroidal hemorrhage after molteno implantation. J Glaucoma. 1996;5(3):170-175. Accessed May 19, 2020.
  7. Oli A, Balakrishnan D. Multimodal imaging in a case of localized suprachoroidal hemorrhage. J Ophthalmic Vis Res. 2020;15(1):104-108. Accessed May 20, 2020. doi: 10.18502/jovr.v15i1.5956.
  8. 8.0 8.1 8.2 8.3 8.4 8.5 Learned D, Eliott D. Management of delayed suprachoroidal hemorrhage after glaucoma surgery. Semin Ophthalmol. 2018;33(1):59-63. doi: 10.1080/08820538.2017.1353814 [doi].
  9. 9.0 9.1 Rezende FA, Kickinger MC, Li G, Prado RF, Regis LG. Transconjunctival drainage of serous and hemorrhagic choroidal detachment. Retina. 2012;32(2):242-249. doi: 10.1097/IAE.0b013e31821c4087 [doi].
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  12. Kurup SK, McClintic JI, Allen JC, et al. Viscoelastic assisted drainage of suprachoroidal hemorrhage associated with seton device in glaucoma filtering surgery. Retina. 2017;37(2):396-399. doi: 10.1097/IAE.0000000000001141 [doi].
  13. Wang L, Yang C, Yang C, et al. Clinical characteristics and visual outcome of non-traumatic suprachoroidal haemorrhage in taiwan. Acta Ophthalmol. 2008;86(8):908-912. Accessed May 19, 2020. doi: 10.1111/j.1755-3768.2008.01266.x.
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